title: Differential responses of components of the autonomic nervous system.
abstract: This chapter conveys several concepts and points of view about the scientific and medical significance of differential alterations in activities of components of the autonomic nervous system in stress and disease. The use of terms such as "the autonomic nervous system," "autonomic failure," "dysautonomia," and "autonomic dysfunction" imply the existence of a single entity; however, the autonomic nervous system has functionally and neurochemically distinctive components, which are reflected in differential responses to stressors and differential involvement in pathophysiologic states. One can conceptualize the autonomic nervous system as having at least five components: the sympathetic noradrenergic system, the sympathetic cholinergic system, the parasympathetic cholinergic system, the sympathetic adrenergic system, and the enteric nervous system. Evidence has accumulated for differential noradrenergic vs. adrenergic responses in various situations. The largest sympathetic adrenergic system responses are seen when the organism encounters stressors that pose a global or metabolic threat. Sympathetic noradrenergic system activation dominates the responses to orthostasis, moderate exercise, and exposure to cold, whereas sympathetic adrenergic system activation dominates those to glucoprivation and emotional distress. There seems to be at least as good a justification for the concept of coordinated adrenocortical-adrenomedullary responses as for coordinated adrenomedullary-sympathoneural responses in stress. Fainting reactions involve differential adrenomedullary hormonal vs. sympathetic noradrenergic activation. Parkinson disease entails relatively selective dysfunction of the sympathetic noradrenergic system, with prominent loss of noradrenergic nerves in the heart, yet normal adrenomedullary function. Allostatic load links stress with degenerative diseases, and Parkinson disease may be a disease of the elderly because of allostatic load.
authors.affiliation: Clinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. Electronic address: goldsteind@ninds.nih.gov.
authors.forename: David S
authors.initials: DS
authors.lastname: Goldstein
mesh_terms: D000818:Animals; D001341:Autonomic Nervous System / Q000033:anatomy & histology / Q000502:physiology* / Q000503:physiopathology*; D001342:Autonomic Nervous System Diseases / Q000503:physiopathology; D049672:History, 19th Century; D049673:History, 20th Century; D049690:History, Ancient; D006801:Humans; D015201:Meta-Analysis as Topic; D018377:Neurotransmitter Agents / Q000266:history / Q000502:physiology*; D010300:Parkinson Disease / Q000503:physiopathology
chemical_list: D018377:Neurotransmitter Agents
keywords: Parkinson disease; Sympathetic nervous system; adrenaline; adrenomedullary; allostatic load; epinephrine; fainting; norepinephrine; syncope